Atrial fibrillation activates AMP-dependent protein kinase and its regulation of cellular calcium handling: potential role in metabolic adaptation and prevention of progression
Background - Atrial fibrillation (AF) is associated with metabolic stress, which activates adenosine monophosphate-regulated protein kinase (AMPK). - Objectives - This study sought to examine AMPK response to AF and associated metabolic stress, along with consequences for atrial cardiomyocyte Ca2+ h...
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| Hauptverfasser: | , , , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
29 June 2015
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| In: |
Journal of the American College of Cardiology
Year: 2015, Jahrgang: 66, Heft: 1, Pages: 47-58 |
| ISSN: | 1558-3597 |
| DOI: | 10.1016/j.jacc.2015.04.056 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.jacc.2015.04.056 Verlag, lizenzpflichtig, Volltext: http://www.sciencedirect.com/science/article/pii/S0735109715021919 
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| Verfasserangaben: | Masahide Harada, Artavazd Tadevosyan, Xiaoyan Qi, Jiening Xiao, Tao Liu, Niels Voigt, Matthias Karck, Markus Kamler, Itsuo Kodama, Toyoaki Murohara, Dobromir Dobrev, Stanley Nattel |
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| 245 | 1 | 0 | |a Atrial fibrillation activates AMP-dependent protein kinase and its regulation of cellular calcium handling |b potential role in metabolic adaptation and prevention of progression |c Masahide Harada, Artavazd Tadevosyan, Xiaoyan Qi, Jiening Xiao, Tao Liu, Niels Voigt, Matthias Karck, Markus Kamler, Itsuo Kodama, Toyoaki Murohara, Dobromir Dobrev, Stanley Nattel |
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| 520 | |a Background - Atrial fibrillation (AF) is associated with metabolic stress, which activates adenosine monophosphate-regulated protein kinase (AMPK). - Objectives - This study sought to examine AMPK response to AF and associated metabolic stress, along with consequences for atrial cardiomyocyte Ca2+ handling. - Methods - Calcium ion (Ca2+) transients (CaTs) and cell shortening (CS) were measured in dog and human atrial cardiomyocytes. AMPK phosphorylation and AMPK association with Ca2+-handling proteins were evaluated by immunoblotting and immunoprecipitation. - Results - CaT amplitude and CS decreased at 4-min glycolysis inhibition (GI) but returned to baseline at 8 min, suggesting cellular adaptation to metabolic stress, potentially due to AMPK activation. GI increased AMPK-activating phosphorylation, and an AMPK inhibitor, compound C (CompC), abolished the adaptation of CaT and CS to GI. The AMPK activator 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) increased CaT amplitude and CS, restoring CompC-induced CaT and CS decreases. CompC decreased L-type calcium channel current (ICa,L), along with ICa,L-triggered CaT amplitude and sarcoplasmic reticulum (SR) Ca2+ content under voltage clamp conditions in dog cells and suppressed CaT and ICa,L in human cardiomyocytes. Small interfering ribonucleic acid-based AMPK knockdown decreased CaT amplitude in neonatal rat cardiomyocytes. L-type Ca2+ channel α subunits coimmunoprecipitated with AMPKα. Atrial AMPK-activating phosphorylation was enhanced by 1 week of electrically maintained AF in dogs; fractional AMPK phosphorylation was increased in paroxysmal AF and reduced in longstanding persistent AF patients. - Conclusions - AMPK is activated by metabolic stress and AF, and helps maintain the intactness of atrial ICa,L, Ca2+ handling, and cell contractility. AMPK contributes to the atrial compensatory response to AF-related metabolic stress; AF-related metabolic responses may be an interesting new therapeutic target. | ||
| 650 | 4 | |a cell calcium handling | |
| 650 | 4 | |a heart pharmacology | |
| 650 | 4 | |a myocardial energy metabolism | |
| 700 | 1 | |a Tadevosyan, Artavazd |e VerfasserIn |4 aut | |
| 700 | 1 | |a Qi, Xiaoyan |e VerfasserIn |4 aut | |
| 700 | 1 | |a Xiao, Jiening |e VerfasserIn |4 aut | |
| 700 | 1 | |a Liu, Tao |e VerfasserIn |4 aut | |
| 700 | 1 | |a Voigt, Niels |e VerfasserIn |4 aut | |
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| 700 | 1 | |a Murohara, Toyoaki |e VerfasserIn |4 aut | |
| 700 | 1 | |a Dobrev, Dobromir |e VerfasserIn |4 aut | |
| 700 | 1 | |a Nattel, Stanley |e VerfasserIn |4 aut | |
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